This review highlights the complex interactions of multiple physiological signals in regulating renin release, emphasizing the need to study integrated responses rather than isolated stimuli.
The various physiological mechanisms that individually modulate the release of renin from the kidney have been reviewed by a number of investigators (18, 27, 68). It is apparent that the juxtaglomerular cells that release renin are influenced by a variety of both stimulatory and inhibitory input signals. The final control mechanisms that govern renin release must process these signals and produce an integrated response. However, the approach to the study of renin release has frequently involved the examination of only a single stimulus, for example renal perfusion pressure, adrenergic activity, or tubular sodium concentration. Moreover, much of this work has been performed with anesthe sized animals, immediately following surgery-when the physiologic state is markedly altered-or in isolated tissue lacking many of the control inputs. Although such experiments provide valuable information, we will primarily review how some of the stimuli for renin secretion interact in homeostatic adjustments in the chronic, unanesthetized dog, in order to elucidate the response of the renin-angiotensin system in man in health and disease. In fact, it was the well-known relationship between renal and cardiac diseases and the possible endocrine role of the kidney that motivated Tigerstedt & Bergman (65) in their discovery of renin.
Gibbons et al. (1984) studied this question.